Complement C3 deficiency leads to accelerated amyloid beta plaque deposition and neurodegeneration and modulation of the microglia/macrophage phenotype in amyloid precursor protein transgenic mice.

Abstract excerpt

Complement factor C3 is the central component of the complement system and a key inflammatory protein activated in Alzheimer's disease (AD). Previous studies demonstrated that inhibition of C3 by overexpression of soluble complement receptor-related protein y in an AD mouse model led to reduced microgliosis, increased amyloid beta (Abeta) plaque burden, and neurodegeneration. To further address the role of C3 in...

Topics

• Alzheimer Disease
• Amyloid beta-Peptides
• Amyloid beta-Protein Precursor
• Animals
• Complement C3
• Humans
• Macrophages
• Mice
• Mice, Inbred C57BL
• Mice, Transgenic